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The relationship between schizophrenia and mother’s vitamin D!



The relationship between schizophrenia and mother's vitamin D!

The relationship between schizophrenia and mother’s vitamin D! Researchers have used molecular imaging technology to confirm the role of vitamin D in the early development of brain cells and say that the origin of schizophrenia may be related to the amount of vitamin D in the mother’s body.

The relationship between schizophrenia and mother’s vitamin D!

In this article we’re going to read about the relationship between schizophrenia and mother’s vi Researchers have used molecular imaging technology to confirm the vital role of vitamin D in the mother’s body for the development of brain cells that produce dopamine, the feel-good chemical in the body.

This finding provides a greater understanding of the underlying mechanisms of neurodevelopmental disorders such as schizophrenia.

Schizophrenia is thought to be caused by a combination of genetic and environmental factors. The exact mechanism by which it does this is unknown, but there is strong evidence that this condition changes the way the brain uses dopamine.

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Scientists hypothesize that exposure to risk factors for schizophrenia during fetal development changes the way dopamine circuits are formed in the brain. Previous studies have shown that low levels of vitamin D in the mother’s body are one of the risk factors that affect the differentiation of dopamine-producing (dopaminergic) neurons into their specialized and mature form.

Now, a group of researchers at the Brain Institute of the University of Queensland, based on past research and with the help of molecular imaging technology, have investigated more closely the relationship between vitamin D, dopaminergic neurons, and schizophrenia.

Scientists created dopamine-like neurons to replicate the differentiation process that occurs during embryonic development. Then these neurons were cultured with and without calcitriol hormone.

Digested vitamin D is inactive until it undergoes two enzymatic reactions in the body. The second reaction occurs in the kidney, where it is converted to calcitriol, the active form of vitamin D. Calcitriol binds to the vitamin D receptor in the cell nucleus and activates it.

Researchers found that vitamin D not only affects cell differentiation but also neuron structure.

“What we found was that the altered differentiation process in the presence of vitamin D not only caused the cells to grow differently but also recruited the machinery to release dopamine differently,” said lead author Daryl Eales.

What these machines mean are neurites, the projections that grow from the cell body of a neuron. Neurites need to send and receive signals to and from other parts of the nervous system.

The researchers found that the number of neurites increased significantly, and in those neurites, the distribution of proteins responsible for the release of dopamine changed. Using a new imaging tool called pseudo-fluorescent neurotransmitters (FFNs), scientists can study how dopamine uptake and release changes in the presence or absence of calcitriol.

FFNs are small molecule dyes that mimic the action of a neurotransmitter such as dopamine. They allow imaging of the storage and release of single molecules in nerve terminals.

The researchers found that compared to the control group, dopamine release was increased in neurons grown in the presence of calcitriol.

“Vitamin D certainly affects the structural differentiation of dopaminergic neurons,” Eales says.

Using FFN to target and observe dopamine molecules means researchers can confirm their long-held belief that vitamin D levels during development affect how dopamine-producing neurons form.

They believe that early changes in dopamine neuron differentiation and function may lead to the dopamine dysfunction seen in adult-onset schizophrenia.

Schizophrenia is a mental disorder characterized by persistent or recurrent episodes of psychosis. Its main symptoms include hallucinations (often auditory hallucinations), delusions, and thought disorders. Other symptoms include social withdrawal, decreased emotional expression, and apathy.

These symptoms usually develop gradually, starting in early adulthood, and in many cases never completely resolve.

There is still no specific test to diagnose it, and it is only diagnosed based on the behavior observed by the patient by a doctor or clinical psychologist along with a history including the reported experiences of the person and the reports of people familiar with the person.

In order to diagnose schizophrenia, doctors must confirm that symptoms and functional disorders have existed in a person for six months. Many people with schizophrenia also have other mental disorders, especially substance abuse disorders, depressive disorders, anxiety disorders, and obsessive-compulsive disorder.

About 0.3 to 0.7% of people are diagnosed with schizophrenia during their lifetime. Estimates in 2017 indicated 1.1 million new cases and in 2019 there were a total of 20 million cases of this disease in the world.

Men suffer from schizophrenia more than women, and the age of onset of the disease in men is on average lower than in women; Although some extensive research has not found gender differences in the prevalence of this disorder.

Possible causes of schizophrenia include genetic factors and environmental factors. Genetic factors include common and rare genetic variants. Possible environmental factors include growing up in the city, marijuana use during puberty, infections, the age of the mother or father, and poor maternal nutrition during pregnancy.

About half of people with schizophrenia make a significant long-term recovery without relapse, and a small proportion of these people recover completely. But the remaining 50% will be disabled for life. In some cases, a person may be hospitalized repeatedly.

Social problems such as long-term unemployment, poverty, homelessness, and abuse of patients and victims are common. The average life expectancy of people with this disorder is 20 years less than the general population. This problem is the consequence of increased physical health problems and a higher suicide rate (about 5%) in schizophrenia patients.

It is estimated that in 2015, around 17,000 people around the world died due to factors related to or caused by schizophrenia.

The main core of the treatment of this disease is the use of antipsychotic drugs, along with psychotherapy, job training, and social rehabilitation. Up to one-third of patients may not respond to first-generation antipsychotics, in which case a second-generation antipsychotic such as clozapine may be used. In situations where doctors determine that there is a risk of harming oneself or others, short-term mandatory hospitalization may be prescribed. Long-term hospitalization is used only in a small number of severe cases of schizophrenia. Longer hospital stays are observed in some countries where supportive services are limited or unavailable.

Finally, schizophrenia is a mental disorder characterized by significant changes in perception, thoughts, behavior, and mood. Schizophrenia symptoms are divided into three categories: positive, negative, and cognitive symptoms. Positive symptoms of schizophrenia are symptoms that are common in other psychotic illnesses and are sometimes referred to as psychotic symptoms. These symptoms may be present in any of the different psychotic disorders, and because they are often transient, they make early diagnosis of schizophrenia difficult.

Now the researchers of the new study plan to investigate whether other environmental risk factors for schizophrenia, such as low oxygen levels or infection during pregnancy, also change the way dopamine neurons develop.

This study was published in the journal Neurochemistry.


Transforming invasive cancer cells into healthy cells!




Transforming invasive cancer cells into healthy cells!

Transforming invasive cancer cells into healthy cells! A specific form of aggressive childhood cancer that forms in muscle tissue may be a new cancer treatment option.

Transforming invasive cancer cells into healthy cells!

Scientists have successfully stimulated rhabdomyosarcoma cells to transform into normal, healthy muscle cells. It’s a breakthrough that could see the development of new treatments for this brutal disease and could lead to similar advances for other types of human cancer.

Rhabdomyosarcoma (RMS) is a highly aggressive type of cancer that arises from mesenchymal cells that have failed to fully differentiate into skeletal muscle myocytes. The tumor cells are identified as rhabdomyoblasts.

“These cells literally turn into muscle, and the tumor loses all of its cancerous characteristics,” says Christopher Wacock, a molecular biologist at Cold Spring Harbor Laboratory. They change from a cell that just wants to use itself more to a cell that is dedicated to contraction, and because all of its energy and resources are now devoted to contraction, it can no longer go back to proliferative and cancerous.

Read More: The genetic signal controlling the blood-brain barrier was discovered

Cancer occurs when cells in different parts of the body mutate. Rhabdomyosarcoma is a type of cancer that is mostly seen in children and teenagers. It usually starts in skeletal muscle when the cells in it mutate and begin to multiply and take over the body.

Rhabdomyosarcoma cancer is aggressive and often fatal, and the survival rate for the moderate-risk group is between 50 and 70%.

One of the promising treatment options for this disease is called “differentiation therapy”. This treatment emerged when scientists realized that leukemia cells are not fully mature and resemble undifferentiated stem cells that have not yet fully transformed into a specific cell type. Differentiation therapy forces those cells to continue growing and differentiate into specific adult cell types.

In a previous study, Wacock and colleagues effectively reversed the mutation in cancer cells that appear in Ewing’s sarcoma.

Ewing’s sarcoma is another cancer that usually appears in the bones in childhood, and is a rare, small, round, blue-colored tumor that occurs in the bones or soft tissue. This tumor can appear in any bone, but it mostly grows in the hip, thigh, arm, shoulder, and ribs, and the age of its prevalence is in adolescence or young adulthood. Ewing is slightly more common in boys than in girls.

The researchers wanted to see if they could replicate their success with rhabdomyosarcoma. At first, they thought that the realization and use of “differentiation therapy” was decades away.

The researchers used a genetic screening technique to narrow down the genes that might force rhabdomyosarcoma genes to continue growing in muscle cells. They found the answer in a protein called nuclear transcription factor-Y (NF-Y).

Rhabdomyosarcoma cells produce a protein called PAX3-FOXO1, which stimulates the proliferation of the cancer and the cancer depends on it.

The researchers found that removing the NF-Y protein inactivated the PAX3-FOXO1 protein, which in turn forced the cells to continue growing and differentiating into mature muscle cells without any signs of cancer activity.

According to the team, this is a key step in the development of a differentiation therapy for rhabdomyosarcoma and could accelerate the realization and expected timing of such therapies.

The researchers say that the positive impact of their technique, which has now been shown on two different types of sarcoma, can be applied to other sarcomas and cancer types as well, as it provides scientists with the tools needed to find out how cancer cells differentiate.

“Every successful treatment has its own story, and research like this is like fertile soil from which new drugs and treatments are born,” says Vakok. 

This research has been published in the journal of the National Academy of Sciences.

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Inventing a lozenge to relieve tooth sensitivity




Inventing a lozenge to relieve tooth sensitivity

Inventing a lozenge to relieve tooth sensitivity. Scientists have developed a way to restore the lost minerals in teeth that cause them to be sensitive.

Inventing a lozenge to relieve tooth sensitivity

What’s worse than not being able to eat delicious treats like ice cream because we don’t want to endure the pain of the cold hitting our sensitive teeth again?

This problem will soon be a thing of the past as researchers have developed a new method of restoring lost tooth minerals that offers a long-term solution to this problem.

Tooth sensitivity, also called dentin hypersensitivity, occurs when the inner dentin layer of the tooth and the tubules within it are exposed, often due to the loss of the tooth’s protective enamel in a process called demineralization. ) they say.

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With the opening of the softer space of the tooth, its nerves, and blood vessels are prone to react to heat, cold, touch, pressure, or acidic foods, which causes pain.

Tooth enamel can be worn away by wear, decay, or grinding and cannot be repaired by natural processes as it is the only non-living tissue in our body.

In recent years, the increase in peroxide-based teeth whitening products has exacerbated tooth enamel wear, and currently, the only way to treat dentin hypersensitivity is to prevent it and treat its symptoms.

Now researchers at the University of Washington have developed a new treatment that can restore lost tooth minerals and provide a permanent solution to the problem of dentin hypersensitivity.

“We [dentists] see patients with sensitive teeth, but we can’t really help them,” says study co-author Sammy Duggan. We all have these restorative options on the market, but they are all temporary because they focus on treating the symptoms and not addressing the root cause.

The goal of researchers is to create a biosimilar, something that closely resembles or mimics the natural biochemical processes that occur in the body. So they focused on a peptide—a short chain of amino acids—that is key to the biological development of human teeth. This peptide, called sADP5, binds to calcium and phosphate ions, the main minerals found in teeth, and uses them to build new mineral microlayers.

In preclinical experiments, the researchers created a small tablet with a core of calcium and phosphate coated in the flavoring agent sADP5, which they tested on dentin discs extracted from human teeth.

Each of the discs had ivory tubes. After three rounds of peptide-guided treatment, the researchers managed to form a new mineral layer on the exposed dentin that stretched into the dentinal tubules and blocked them.

“Our technology recreates the same minerals found in teeth, including enamel, cementum, and dentin, that were previously dissolved through demineralization,” said Deniz Yusisoy, lead author of the study.

He added: the newly formed mineral microlayers close the channels of communication with the nerves of the tooth, and after that excessive sensitivity does not cause a problem anymore.

By measuring the hardness of the newly formed mineralized layer, the researchers found that it was significantly harder than non-mineralized, natural human dentin. Also, by testing it using the thermal wear method, the mineral layer was not separated from the tooth.

Both of these findings show that this method can provide resistance to long-term mechanical and thermal stresses that teeth face in the natural environment of the mouth. In addition to tablets, researchers have included their peptide-based formula in mouthwashes, tooth gels, teeth whiteners, and toothpaste.

Hanson Fong, one of the authors of the study, says: “There are many methods of design and delivery. The most important thing is the peptide, which is a key ingredient in our formula and works.

Further research is needed to investigate the permeability and chemical stability of the mineral layer to achieve an effective and easy-to-use treatment for dentin hypersensitivity, including the implementation of the peptide-guided approach in vitro.

The study was published in the journal ACS Biomaterials Science & Engineering.

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The genetic signal controlling the blood-brain barrier was discovered




The genetic signal controlling the blood-brain barrier was discovered

The genetic signal controlling the blood-brain barrier was discovered. In a new study, researchers have succeeded in identifying a genetic signal that controls the blood-brain barrier.

The genetic signal controlling the blood-brain barrier was discovered

New research in mice and zebrafish has discovered the genetic signal needed to form and maintain the blood-brain barrier.

The discovery could allow scientists to control the permeability of the blood-brain barrier and provide a more effective way to deliver drugs to the brain to treat stroke, neurological and psychiatric diseases, and cancer.

The blood-brain barrier (BBB) is a highly interconnected system of specialized cells that form a layered, semipermeable membrane that serves a dual purpose: protecting against toxins or pathogens entering the brain from the bloodstream while allowing passage through itself. gives vital nutrients.

Read More: The relationship between schizophrenia and mother’s vitamin D!

The blood-brain barrier is the separating area between the extracellular fluid of the brain in the central nervous system and the circulating blood flow in the body so that if colored substances are injected into the blood, it can be seen that there is no trace of this substance inside the brain. This curtain or barrier is made up of special capillaries, which, unlike the normal structure of capillaries, do not have the usual pores, and the intercellular connection in them is tight, and as a result, many molecules and micromolecules, as well as bacteria, are able to pass through them (through Diffusion) and reaching the cerebrospinal fluid is not in the brain. Conversely, the endothelial surface of these capillaries is covered with special proteins that allow glucose to enter the brain as nutrition. Also, gas exchange (oxygen-carbon dioxide) between circulating blood and the brain can be done without any problem through this barrier.

But the protective function of the blood-brain barrier can prevent effective drugs from being delivered to the brain to treat cancer, stroke, or neurological diseases such as Parkinson’s or Alzheimer’s.

Over the years, various methods have been developed to increase the permeability or leakiness of the blood-blood barrier to enable the delivery of drug therapies, including the use of magnetic nanoparticles, ultrasound, and engineered fat cells.

Now, a new study by Harvard Medical School researchers has identified a gene that produces a signal necessary for the development and maintenance of the blood-brain barrier and may provide a way to control its permeability.

Researchers have long known that the permeability of the blood-brain barrier is controlled by surrounding cells, but the genes in those cells remain unknown. Of course, when the researchers in the current study began to investigate the blood-brain barrier in zebrafish, the answers to these questions became clear.

In previous studies on transparent zebrafish, researchers discovered a gene called mfsd2aa that, when mutated, caused the blood-brain barrier to leak throughout the brain. But in some zebrafish, this barrier was permeable only in the forebrain and midbrain, not in the hindbrain.

“This observation led me to find a gene that makes the blood-brain barrier more permeable,” says Natasha O’Brown, lead author of the study.

In the present study, the researchers conducted additional experiments on zebrafish and mice. They found that region-specific breakdown of the blood-brain barrier is associated with mutations in the spock1 gene, which is expressed in nerve cells throughout the retina, brain, and spinal cord, but not in cells that form the blood-brain barrier.

They observed that spock1 mutant animals had more vesicles in their endothelial cells, which are key components of the blood-brain barrier. Vesicles are bubble-like membranes that store and transport cellular products and can transport large molecules across the blood-brain barrier. They also have a smaller basement membrane, which is a network of proteins found between endothelial cells and pericytes, cells that are important for forming blood vessels and maintaining the blood-brain barrier.

RNA analysis showed that spock1 alters gene expression in endothelial cells and pericytes in the blood-brain barrier, but not in other brain cell types.

When the human Spock1 protein was injected into the zebrafish brain, the endothelial cells and pericytes were repaired at the molecular level and restored about 50% of the blood-brain barrier function.

Based on this discovery, the researchers concluded that the Spock1 protein produced by neurons begins to form the blood-brain barrier during embryonic development and helps maintain it during adulthood.

“Spock1 is a potent secreted neurosignal that can promote and induce barrier properties in these blood vessels,” says O’Brown. Without it, you don’t have a functional blood-brain barrier.

The researchers say their study provides a more complete picture of the permeability of the blood-brain barrier and opens the door to the development of therapies that target spock1, potentially improving the treatment of neurological disorders such as Parkinson’s and Alzheimer’s and psychiatric disorders.

This is not the first neural signal that scientists have found, but it is the first signal from neurons that appears to specifically regulate inhibitory properties, Oberon says. I think this discovery gives us a powerful tool to try and change.

The researchers continue to look at how different pericytes are affected by spoc1 signaling. They would like to see if administering spock1 can counteract the effects of stroke on the blood-brain barrier.

This study was published in the journal Developmental Cell.

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